Weed populations respond and adapt to herbicide stress by evolving resistance. Glyphosate resistance is primarily caused by the amplification of the target site gene, EPSPS, where multiple copies produce a large enough protein pool so that field rates do not kill the plant. This mechanism has evolved independently in at least nine divergent weed species. It has been demonstrated that EPSPS gene duplication may be transposon mediated in Kochia scoparia. A key regulator of transposable element (TE) activity is DNA methylation. The role of the epigenome and subsequent transcriptome in transient responses to herbicides of their primary target, weeds, is not well understood.In this study, we performed RNA-Seq and bisulfite sequencing on leaf tissue from glyphosate-sensitive kochia before and three weeks after treatment with two sublethal doses to determine if glyphosate causes hypomethylation of the genome, allowing for the activation of transposons and upregulation of stress-related genes. Our results shows that overall gene expression was suppressed by glyphosate and increases in CHH methylation through development were also ceased. We did not observe significant global changes in cytosine methylation, and overall responses were stochastic. When combining the two datasets together, there was no direct correlation between changes in methylation and changes in gene expression suggesting that DNA methylation is not the primary cause of differential expression in our study. Our results broaden the knowledge pool of weedy species epigenomics and aid in understanding the contribution of DNA methylation to plant resilience in response to herbicide stress.
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